AVP is a hormone primarily involved in water transport. This effect has been shown to be mediated by stimulation of receptors in the renal collecting tubule, so called V2 receptors. The proposed study aims to determine whether arginine vasopressin (AVP) plays a physiologic role in maintaining potassium and acid-base in human subjects. Specifically, we wish to test the hypothesis that (a) AVP increases both renal potassium and acid excretion by stimulation of V2 receptors in the collecting tubule; (b) dietary potassium loading and ammonium chloride loading stimulate AVP secretion while dietary potassium deprivation has the opposite effect; and (c) potassium deprivation will impair the kaliuretic response to AVP, much the same way it impairs the hydroosmotic response to AVP, while dietary potassium loading will enhance it. Thus, alterations in AVP secretion and amplification/suppression of its renal actions are postulated as possible mechanisms whereby potassium and acid-base balance can be maintained under conditions where dietary intake of potassium and acid are modified. To test this hypothesis, we shall conduct a three-phase study in healthy subjects with normal kidney function. First, we shall determine if AVP increases potassium excretion and distal urinary acidification and explore the mechanism (s) of these effects. Secondly, the effect of potassium loading, potassium deprivation and metabolic acidemia on AVP secretion will be assessed by the response of plasma AVP secretion to an osmotic stimulus. Thirdly, the effect of prior potassium surplus and prior potassium deprivation on the renal potassium excretory and acidification responses to the infusion of physiologic amounts of AVP will be assessed.